Toward an Epistemology of Evolution

The influence of humans on the Earth, our inherent dependence on it, our relationship to each other, and our connection to all life — no discipline meaningfully illuminates such statements as biology does. Biology unveils the substance that serves as the blueprint for our own construction, but also demonstrates how that substance is life’s very deepest homology. That is to say, biology can offer explanation at multiple levels: first by establishing patterns and investigating their creative processes, and then by providing proximate and ultimate causes for observed patterns and processes. This dual causality — the proximate functional ‘how’ and the ultimate evolutionary ‘why’ — is both particular and of particular importance to biological sciences; the ‘why’ being the stuff that gives the ‘how’ consequence. So what does this mean for the student of biology?

DiSessa, A. A. (1993). Toward an epistemology of physics. Cognition and instruction, 10(2-3), 105-225.
Mayr, E. (1961). Cause and effect in biology. Science, 134(3489), 1501-1506.

Evolution-Centered Teaching

A robust conceptual framework in biological sciences requires understanding evolutionary principles. And yet, postsecondary biology courses are often taught as a string of facts and examples devoid of connection, relegating evolutionary prinicples to the course dedicated to evolution. This divorces the most compelling aspects of biology — the discipline's framework and narrative — from the teaching and learning of biology. Instead, we must frame each course in its appropriate evolutionary framework and work to draw connections between sub-disciplines.

The Four Causes of Adaptation

This project spans four BIOS courses (BIOS 120, BIOS 331, BIOS 343, and BIOS 430) and includes more than 500 student participants. The purpose is to aid in improving conceptual understanding of biological principles — and by extension biology instruction at UIC — by examining how students think about complex and multilayered biological questions.

Hundreds of studies indicate that students maintain tenacious misconceptions regarding the evolutionary principles necessary for recognizing levels of biological explanation. To dissect these misconceptions, I administered a pre-post assignment with open-ended reflective questions to explore (1) how students construct explanations about natural selection and adaptation across several levels of postsecondary study, and (2) the extent to which their explanations change as they continue formal biology instruction. My framework, adapted from Tinbergen’s Four Questions, categorizes students’ answers based on the level of explanation addressed. I also catalog common naïve intuitions in tandem (e.g., teleological, anthropocentric, or Lamarckian inheritance).

Preliminary results: I find that levels of explanation and naïve intuitions shift regularly within and between student responses, and that continued formal instruction does not nudge students’ explanations toward the dominant conceptions in the field. I discuss the implications of these findings for both teaching and biology education generally: namely, that we must do better in teaching students how to think about biology by providing them with a more robust framework and narrative structure.

Dual Causality in Biology

Unlike other disciplines, varying levels of causation account for biological phenomena. That is to say, biology is a “historical science” — information coded in the genes of living organisms is necessarily historical (inherited) information. Moreover, varying proximate or ultimate processes may account for similar observed patterns. For a robust understanding of any given pattern or phenotype, individual-level (proximate, functional) processes must also be evaluated against species-level (ultimate, evolutionary) processes. So what does the dual causality of biology mean for complex problems like cancer or the evolution of sex?

On cancer and natural selection

Cancer is a phenotype: many proximate processes may account for it, but its dynamics share many features across individuals. As such, a growing body of research aims to understand and treat cancer by viewing carcinogenesis as a speciation event inside the host, giving rise to a new parasitic organism. This organism is subject to the same evolutionary and ecological dynamics as all others — that is, cancer evolves in response to its environment through a combination of stochastic and deterministic forces. Viewing cancer through this “ultimate” lens opens up tremendous opportunity for future research and therapies. Yet a frequent question is often raised in response to this idea: if cancer is adaptive, why does it kill its host?

There are a variety of theoretical models that suggest several ways in which natural selection or individual adaptations can be detrimental to a population overall. Empirical evidence from the bacterium Myxococcus xanthus has demonstrated that artifically selected “cheater” strains invade wild-type strains, ultimately causing the extinction of the entire population (Fiegna and Velicer 2003). Yet natural selection is commonly misunderstood as an optimization process that works for the “overall good of the species.” This misconception is tenacious, perhaps in response to the overwhelming variety of organisms that appear perfectly designed to suit their environment. But this is not the case — natural selection may be non-random, but is not goal-driven or forward-thinking.